2022-06-16 スイス連邦工科大学ローザンヌ校(EPFL)
科学者たちは、エストロゲンとプロゲステロンという両方のホルモンが腫瘍の成長を促進し、複合的な治療が実際に転移を促進することを発見したのです。
異なる患者の腫瘍は、2つのホルモンに対する反応が異なることを発見し、内分泌療法は、個人に合わせて改善できる可能性があることを示唆しています。
さらに、プロゲステロン受容体の発現を阻害することが治療の選択肢になり得ます
<関連情報>
- https://actu.epfl.ch/news/breakthrough-study-of-hormone-crosstalk-in-breast-/
- https://www.nature.com/articles/s41467-022-30898-0
エストロゲン受容体陽性乳がんは、患者固有のホルモン感受性を持ち、プロゲステロン受容体に依存する。 Estrogen receptor positive breast cancers have patient specific hormone sensitivities and rely on progesterone receptor
Valentina Scabia,Ayyakkannu Ayyanan,Fabio De Martino,Andrea Agnoletto,Laura Battista,Csaba Laszlo,Assia Treboux,Khalil Zaman,Athina Stravodimou,Didier Jallut,Maryse Fiche,Philip Bucher,Giovanna Ambrosini,George Sflomos & Cathrin Brisken
Nature Communications Published:06 June 2022
DOI:https://doi.org/10.1038/s41467-022-30898-0
Abstract
Estrogen and progesterone receptor (ER, PR) signaling control breast development and impinge on breast carcinogenesis. ER is an established driver of ER + disease but the role of the PR, itself an ER target gene, is debated. We assess the issue in clinically relevant settings by a genetic approach and inject ER + breast cancer cell lines and patient-derived tumor cells to the milk ducts of immunocompromised mice. Such ER + xenografts were exposed to physiologically relevant levels of 17-β-estradiol (E2) and progesterone (P4). We find that independently both premenopausal E2 and P4 levels increase tumor growth and combined treatment enhances metastatic spread. The proliferative responses are patient-specific with MYC and androgen receptor (AR) signatures determining P4 response. PR is required for tumor growth in patient samples and sufficient to drive tumor growth and metastasis in ER signaling ablated tumor cells. Our findings suggest that endocrine therapy may need to be personalized, and that abrogating PR expression can be a therapeutic option.
